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Hashimoto Thyroiditis
Introduction
Hashimoto thyroiditis is an autoimmune disease that destroys thyroid follicular cells through cell- and antibody-mediated immune processes. This disease is also known as chronic autoimmune thyroiditis and chronic lymphocytic thyroiditis. Hashimoto thyroiditis is the most common cause of hypothyroidism in developed countries.[1] The pathophysiology of this disease involves the formation of antithyroid antibodies and T-cell activation that attack the thyroid tissue, causing progressive fibrosis. Together with Graves disease, this condition comes in the category of autoimmune thyroid disorders.[2] This condition was initially described by a Japanese physician, Haruto Hashimoto, in 1912 as "struma lymphomatosa" after he found enlarged thyroids having lymphocytic infiltration.[3]
Women are more commonly affected. The female-to-male ratio is at least 7 to 10:1.[4] The incidence of Hashimoto thyroiditis increases with age, with most cases found between ages 45 and 55 years. The incidence tends to be higher in countries with a lower prevalence of iodine deficiency.[2] Hashimoto thyroiditis can occur alone, or it can occur as a part of autoimmune polyglandular syndrome (APS).[5] Some individuals with Graves disease might transform into Hashimoto thyroiditis and vice versa. This could indicate a common pathogenesis for these disorders but different clinical presentations.[6][7][8][9]
Etiology
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Etiology
The underlying etiology of Hashimoto thyroiditis is still not fully understood but is thought to be a combination of genetic and environmental factors.
Genetic Factors
Hashimoto thyroiditis has been shown to have a strong familial predisposition with disease clustering in families, including some members developing Graves disease. A Danish study had shown a 50% concordance rate for Hashimoto thyroiditis and 80% for thyroid antibody positivity in monozygotic twins.
Several genes, including those encoded by the human leukocyte antigen (HLA) complex, immune regulatory genes (CD40, FoxP3, CD25, CTLA-4, and PTPN22), and thyroid-specific genes (TSH receptor and thyroglobulin), are linked to the development of Hashimoto thyroiditis.[10][11] Furthermore, Hashimoto thyroiditis is more common in individuals with Turner syndrome and Down syndrome.[12][13]
Environmental Factors
Since only 50% of the monozygotic twins in a Danish study were shown to have concordance for Hashimoto thyroiditis, environmental factors seem to have an essential role in the development of Hashimoto thyroiditis.[14]
Hygiene hypothesis
Similar to many allergic and autoimmune conditions, individuals living in a more hygienic environment with less exposure to microbial agents seem to have a higher incidence of Hashimoto thyroiditis.[15]
Iodine status
Mild iodine deficiency has been associated with a lower prevalence of Hashimoto thyroiditis, whereas chronic exposure to excess iodine intake has been associated with a higher prevalence of Hashimoto thyroiditis. This is partly because highly iodinated thyroglobulin creates a more immunogenic intrathyroid environment.[16][17][18] Significant iodine deficiency also increases thyroid autoimmunity.[19][18][16]
Selenium status
Selenoproteins are essential for thyroid function and protection.[20][21] The important thyroidal selenoproteins are the iodothyronine deiodinases, glutathione peroxidases, and thioredoxin reductases. These enzymes are involved in thyroid hormone metabolism, maintenance of cellular metabolism and regulation of redox state, and protection from oxidative damage from reactive oxygen species and hydrogen peroxide.[22][23] Deficiency in this mineral has been associated with a higher risk of Hashimoto thyroiditis. A systematic review and meta-analysis from 2024 showed that thyroid antibody levels were reduced with selenium supplementation, independent of underlying selenium deficiency and thyroid hormone replacement. Thyroid-stimulating hormone (TSH) levels also reduce with selenium supplementation, independent of thyroid hormone replacement. The certainty of this evidence was moderate.[24]
Iron status
Thyroid peroxidase is an enzyme that contains heme (iron). Hence, the presence of iron deficiency can impair thyroid activity and also increase thyroid autoimmunity.[16][25] Individuals with Hashimoto thyroiditis are at higher risk for comorbid conditions like celiac disease and autoimmune gastritis, which are often associated with iron deficiency.[26][27] Women of reproductive age are also at high risk for developing iron deficiency due to blood loss during menstruation.[28]
Vitamin D status
Vitamin D has been established as an important immunomodulator.[29] Individuals with vitamin D deficiency have higher thyroid antibody levels, possibly contributing to Hashimoto thyroiditis development and its progression.[30][31] The association of vitamin D receptor polymorphisms with thyroid autoimmunity has shown conflicting results.[32]
Role of gut microbiome
The gut microbiota regulates the immune system and contributes significantly to thyroid hormone metabolism. Hence, alterations in the gut microbiome can increase the risk of thyroid autoimmunity.[33][34][35][36] Whether the alteration in the gut microbiome occurs before or after the development of Hashimoto thyroiditis is unclear. A cross-sectional study, including euthyroid individuals, showed no robust difference in gut microbiome between individuals with or without thyroid peroxidase antibodies regarding alpha and beta diversity.[37]
Epidemiology
Hashimoto thyroiditis is the most common cause of hypothyroidism in the United States and in those areas of the world where dietary iodine intake is adequate.[38] A systematic review and meta-analysis, including studies from multiple countries, found the overall global prevalence of Hashimoto thyroiditis to be 7.5%, higher in low-middle-income areas at 11.4%.[39] Additionally, the prevalence in women was 4 times that in men.[39]
Almost 10% of the population in the United States has been shown to have positivity for thyroid antibodies. Various studies have found the prevalence of thyroid antibody positivity in the general population between 5% to 20%.[40][41][42][43][44] Thyroid peroxidase antibodies are present in 5% to 14% of pregnant females, whereas thyroglobulin antibodies are present in 3% to 18% of pregnant females.[45]
Pathophysiology
The presence of lymphocytic infiltration and fibrosis in the thyroid follicles are characteristic of Hashimoto thyroiditis. Both cellular (T-cell mediated) and humoral (B-cell mediated) immune responses have essential roles in the pathogenesis of this disorder.[46]
Role of B Cells
Individuals with Hashimoto thyroiditis have the following polyclonal [47] antibodies specific to thyroid antigens:
- Thyroid peroxidase antibody: This is the most common antibody found in Hashimoto thyroiditis. These are found in over 90% of individuals with Hashimoto thyroiditis.[48][49]
- Thyroglobulin antibody: This is present in 50% to 80% of the individuals with Hashimoto thyroiditis.[48][50]
- TSH receptor antibody (TSHR Ab): Various types of TSHR Ab have been identified. These can be stimulating, blocking, or neutral.[51][52][53] A vast majority of TSHR Ab in Hashimoto thyroiditis is the blocking type. Rarely can individuals with Hashimoto thyroiditis have TSHR-stimulating antibodies, which can also result in thyroid eye disease. This might also explain why few individuals with Hashimoto thyroiditis switch to Graves disease.[54]
Role of T Cells
CD8+ T cells are a central part of the immune dysfunction underlying the pathogenesis of Hashimoto thyroiditis. These cytotoxic cells infiltrate the thyroid tissue, causing inflammation and destruction of the follicular cells.[55]
CD4+ T cells activate other immune cells, especially macrophages and B cells, which lead to the production of autoantibodies.[46] Different subsets of CD4+ T cells, including Th1, Th2, Th17, and Tregs (regulatory T cells), have various functions, and their imbalance contributes to the pathogenesis of Hashimoto thyroiditis.[56] Th1 is upregulated in Hashimoto thyroiditis, promoting inflammation in the thyroid tissue. Tregs are critical in promoting immune tolerance and avoiding excessive immune responses. Tregs are downregulated in Hashimoto thyroiditis.[57]
Histopathology
The most commonly described histopathological abnormality in Hashimoto thyroiditis is lymphocytic infiltration and destruction of follicular cells (see Image. Hashimoto Thyroiditis).[58][59] Immune cells commonly include lymphocytes and plasma cells, while others include macrophages and, occasionally, giant cells.[59] The presence of fibrotic tissue is typically noted. Lymphoid follicles containing Hurtle cells and large follicular-derived cells, also called Askanazy cells, with eosinophilic granules, are often present.[60][61]
Histopathological variants of Hashimoto thyroiditis have been described, including:
History and Physical
Individuals with Hashimoto thyroiditis have varying presentations.
Hyperthyroidism or Hashitoxicosis
A small proportion of individuals with Hashimoto thyroiditis present with hyperthyroidism. This condition is known as Hashitoxicosis. This likely occurs due to the destruction of the follicular cells, leading to leakage of prestored thyroid hormones into the bloodstream. This hyperthyroid is usually transient. This presentation is similar to subacute thyroiditis. These individuals could be at risk of developing permanent hypothyroidism.[68][69][70] A small percentage of individuals with Hashimoto thyroiditis might switch to Graves disease and present with hyperthyroidism after being hypothyroid for years before the switch.[71][72]
Euthyroid State
A majority of individuals with Hashimoto thyroiditis are euthyroid with normal thyroid function tests. About 20% to 30% of individuals with Hashimoto thyroiditis develop hypothyroidism.[73]
Subclinical Hypothyroidism
These individuals have elevated TSH, usually less than 10 mIU/L, with normal T4 and T3 levels.[74][75]
Overt Hypothyroidism
These individuals present with symptoms of hypothyroidism, a TSH of more than 10 mIU/L, or low T4 and T3 levels. Usual symptoms include fatigue, unintentional weight gain, cold intolerance, constipation, changes in menstrual cycles (typically heavy menstruation), hair loss, brittle nails, confusion, and brain fog. Individuals might notice puffiness around the eyes, ankle swelling, voice changes, muscle aches/weakness, neuropathy, and joint aches.[76][77][78]
Thyroiditis
Thyroiditis can manifest in painless and painful variants. Thyroid inflammation results in transient thyrotoxicosis, a rare manifestation of Hashimoto thyroiditis. Most cases are painless. A few may be accompanied by throat pain. These cases are resolved within a few months.[79] Rare reports on prolonged or recurrent painful thyroiditis have been published, with some individuals even needing thyroidectomy.[80][81][82]
Reproductive Effects in Women
Women may be found to have Hashimoto thyroiditis if they suffer recurrent miscarriages and/or inability to conceive. Hashimoto thyroiditis can also impair assisted conception.[83][84][85] The effects of hypothyroidism on fertility and pregnancy are not discussed in this article.
Postpartum Thyroiditis
Postpartum thyroiditis is a condition in postpartum women that usually develops around 6 months after childbirth, but it can occur anytime within a year in the postpartum phase. This condition is mostly seen in women who have underlying Hashimoto thyroiditis, most likely due to the rebound of immune response after pregnancy, which can result in an exaggerated autoimmune response destroying thyroid follicular cells. Postpartum thyroiditis is usually transient, but a few women might develop permanent hypothyroidism.[86][87]
Thyroid Nodularity
Ongoing inflammation in the thyroid gland in Hashimoto thyroiditis leads to the development of thyroid nodules. Around 20% to 30% of individuals with Hashimoto thyroiditis have thyroid nodules, and the incidence increases with age.[88] Some individuals may have compressive neck symptoms (dysphagia, dyspnea, dysphonia, chronic cough, and/or pressure) due to the development of thyromegaly with or without thyroid nodularity.
Eye Involvement
Up to 6% of individuals with Hashimoto thyroiditis can be affected by thyroid eye disease.[54] About 15% of individuals with Hashimoto thyroiditis have TSHR Ab. Most of these are the blocking type. A small proportion of individuals can have TSHR-stimulating antibodies, resulting in eye involvement.[54][88][89]
Evaluation
Laboratory Studies
The following laboratory studies may be used for diagnostic evaluation of thyroid function and identification of comorbid conditions:
- Thyroid function tests: TSH, T4, and T3 levels should be tested to assess thyroid function.
- Thyroid antibodies: Thyroid peroxidase antibody is positive in over 90% of cases, whereas thyroglobulin antibody is positive in 50% to 80% of cases. Elevated thyroid antibodies correlated with disease activity.[90] Individuals with thyroid antibody positivity have a high probability of developing overt hypothyroidism, whereas individuals with negative antibody levels are more likely to present with subclinical hypothyroidism. A positive family history is also more likely when thyroid antibodies are elevated. These individuals are also more likely to have larger thyroid gland size.[91][50] If a patient presents with thyroid eye disease, TSH receptor antibody levels should be assessed.
- Iron studies: Serum iron levels should be checked in individuals with clinical symptoms of iron deficiency and gastrointestinal symptoms due to the higher prevalence of celiac disease and atrophic gastritis in individuals with Hashimoto thyroiditis.
- Vitamin D level: Vitamin D status should be assessed due to an increased incidence of vitamin D deficiency in individuals with thyroid disorders.[92]
Imaging Studies
A thyroid ultrasound can be performed if thyroid enlargement or nodularity is noted on physical examination or if the patient has compressive symptoms.
Treatment / Management
Current clinical guidelines emphasize disease management rather than prevention or cure.
Thyroid Hormone Replacement
The mainstay of treatment for hypothyroidism that develops due to Hashimoto thyroiditis is thyroid hormone replacement. The drug of choice is titrated levothyroxine sodium administered orally, which has a half-life of 7 days and can be given daily. Levothyroxine sodium, which is best taken early in the morning on an empty stomach for optimum absorption, should not be taken with iron or calcium supplements, aluminum hydroxide, and proton pump inhibitors to avoid suboptimal absorption.
The standard dosage is 1.4 to 1.8 µg/kg per day, but this can vary from one patient to another. Individuals younger than 60 should be commenced on a standard full dose if TSH >20 mIU/L; however, lower doses should be used in patients with cardiovascular diseases and older adults. In patients older than 60, the recommended starting dose is 25 µg/day, with reevaluation in 6 to 8 weeks. In contrast, in pregnancy, the dose of thyroxine needs to be increased by 30%. In patients with short-bowel syndrome and malabsorption, increased doses of levothyroxine are required to maintain a euthyroid state.[93](A1)
Treatment in euthyroid women
Some experts will recommend initiating levothyroxine in women with TSH >2.5 with or without a history of pregnancy loss and in women using assisted reproductive measures.
Role of selenium supplementation
Recent systematic reviews and meta-analyses showed modest benefits in managing Hashimoto thyroiditis in individuals without thyroid hormone replacement, with improved thyroid function parameters and reduced thyroid antibodies.[24][94] More research is needed to establish clear benefits. Selenium supplementation of 50 to 100 µg daily could be helpful and safe, especially in areas with selenium deficiency.[95] A study including 412 individuals showed an improvement in quality of life parameters with selenium supplementation (200 µg/daily) in individuals on levothyroxine for management of hypothyroidism due to Hashimoto thyroiditis.[96](A1)
Iron deficiency treatment
Every unit increase in iron level has been demonstrated to decrease the risk of Hashimoto thyroiditis by 43% in women of reproductive age.[97](B2)
Vitamin D deficiency treatment
Correction of vitamin D deficiency may be helpful, though more large-scale studies are needed to establish clear benefits. Two small randomized controlled clinical trials have shown reduced thyroid antibody levels and improved TSH levels. Individuals with vitamin D deficiency were included in these trials. One trial based in India gave individuals in the intervention group a high dose of cholecalciferol, 60,000 IU, for 8 weeks.[98] The other trial, based in China, showed a group of individuals treated with cholecalciferol 800 IU daily compared to another group treated with cholecalciferol 800 IU daily and levothyroxine 25 to 50 µg/daily for 6 months.[99] (A1)
Furthermore, in another study in Greece, 186 vitamin D-deficient individuals were given 1200 to 400 IU of cholecalciferol daily for 4 months, with a reduction seen in thyroid peroxidase antibody levels.[100] A systematic review and meta-analysis including 862 individuals also showed the positive effect of vitamin D supplementation on thyroid function and reduction in antibody levels.[101](A1)
Dietary modifications
Limited evidence supports the benefits of an autoimmune or anti-inflammatory diet in the management of thyroid disorders. The theory behind the inflammation involves leaky gut syndrome, where an insult to the gut mucosa allows the penetrance of proteins that do not typically enter the bloodstream via transporters in the gut mucosa. Experts have theorized that a response similar to molecular mimicry occurs, and antibodies are produced against the antigens. Unfortunately, the antigen may be structurally similar to thyroid peroxidase, leading to antibody formation against this enzyme.
The concept of an autoimmune diet is based on healing the gut and decreasing the severity of the autoimmune response.[102] More research is required on this topic before becoming a component of established guidelines. A small study, which included 40 female subjects, showed positive effects on thyroid function and lower thyroid peroxidase and thyroglobulin antibody levels by following a Mediterranean and gluten-free diet.[103](A1)
Differential Diagnosis
Differential diagnoses that should be considered when evaluating Hashimoto thyroiditis:
- Euthyroid sick syndrome
- Goiter
- Graves disease (diffuse toxic goiter)
- Hypopituitarism (panhypopituitarism)
- Lithium-induced goiter
- Nontoxic goiter
- Polyglandular autoimmune syndrome type 1
- Polyglandular autoimmune syndrome type 2
- Thyroid cancer (lymphoma)
- Toxic nodular goiter
Prognosis
Many individuals with Hashimoto thyroiditis are euthyroid, but they are at a higher risk for developing overt hypothyroidism in the future. The risk of developing hypothyroidism increases by 5% every year.[104] These individuals with Hashimoto thyroiditis should have thyroid function testing done annually.
Complications
Thyroid malignancy: Whether Hashimoto thyroiditis is associated with an increased risk of papillary thyroid carcinoma remains unclear.[105] The effect of the presence of Hashimoto thyroiditis on the outcomes of papillary thyroid carcinoma is also conflicting.[106][107] Individuals with Hashimoto thyroiditis are at risk for a rare thyroid malignancy: primary thyroid lymphoma. The incidence of primary thyroid lymphoma is 0.5% to 5% of all thyroid malignancies.[108][109][110][111]
Deterrence and Patient Education
Hashimoto thyroiditis is an autoimmune disorder involving the thyroid gland that can result in thyroid dysfunction and the development of hypothyroidism. This disorder has a high familial predisposition. Individuals with Hashimoto thyroiditis are at twice the risk of developing an underactive thyroid compared to those without it.
Thyroid hormone replacement is only recommended in individuals with overt hypothyroidism. Treatment of subclinical hypothyroidism can be considered in select cases with significant symptoms of hypothyroidism affecting the quality of life of women of reproductive age, especially if they are trying to conceive. Many individuals living in iodine-replete areas might take iodine supplements for their thyroid health. Excess iodine supplementation tends to worsen Hashimoto thyroiditis. Maintenance of normal iron and vitamin D levels might improve thyroid function and reduce antibodies in Hashimoto thyroiditis. Selenium supplementation can be considered in individuals with autoimmune thyroid living in areas with selenium-deficient soil.
Pearls and Other Issues
Hashimoto thyroiditis is one of the most frequent autoimmune diseases and has been reported to be associated with gastric disorders in 10% to 40% of patients. According to research by Cellini et al, about 40% of patients with autoimmune gastritis also present with Hashimoto thyroiditis. Chronic autoimmune gastritis is characterized by the partial or complete disappearance of parietal cells, leading to impairment of hydrochloric acid and intrinsic factor production. The patients go on to develop hypochlorhydria-dependent iron-deficient anemia, which leads to pernicious anemia and severe gastric atrophy.
Thyrogastric syndrome was first described in the 1960s when thyroid autoantibodies were found in a subset of patients with pernicious anemia and atrophic gastritis. The latest guidelines have incorporated the 2 aforementioned autoimmune disorders into a syndrome now known as polyglandular autoimmune syndrome. This is characterized by 2 or more endocrine and nonendocrine disorders. The thyroid gland develops from the primitive gut; therefore, the thyroid follicular cells share similar characteristics with parietal cells of the same endodermal origin. For example, both are polarized and have apical microvilli with enzymatic activity, and both can concentrate and transport iodine across the cell membrane via the sodium/iodide symporter. Iodine not only plays an essential role in the production of thyroid hormone but is also involved in regulating gastric mucosal cell proliferation, acts as an electron donor in the presence of gastric peroxidase, and assists in removing free oxygen radicals.
Notably, due to the pharmaceutical formation of thyroxine available worldwide, there can be absorption problems in patients with gastric mucosa disorders. Most levothyroxine is obtained by salification with sodium hydroxide, making sodium levothyroxine. The absorption of T4 occurs in all areas of the small intestine and ranges from 62% to 84% of the ingested dose. Decreased gastric acid secretion can disrupt this percentage and may cause issues with reduced absorption of most pharmaceutical-grade forms of levothyroxine, except for liquid-based or soft gel formations.
Clinicians should note the association between thyroid and gastric autoimmune diseases. Iron deficiency anemia and thyroxine absorption issues should encourage further diagnostic workup.
Enhancing Healthcare Team Outcomes
Effective management of Hashimoto thyroiditis requires a collaborative, interprofessional approach to ensure patient-centered care, improve outcomes, and enhance patient safety. Physicians, including endocrinologists, primary care clinicians, and internists, play a crucial role in diagnosing and monitoring the disease, adjusting levothyroxine therapy based on individual needs, and screening for complications such as lymphoma. Advanced practitioners and nurses provide ongoing patient education, reinforcing the importance of adherence to treatment, recognizing symptoms of hormone imbalance, and scheduling regular follow-ups for thyroid function testing. Pharmacists contribute by reviewing medication interactions, counseling patients on proper levothyroxine administration, and ensuring safe and effective dosing to prevent hormone toxicity.
Interprofessional communication and care coordination are essential to optimizing team performance and patient outcomes. Clear communication among clinicians allows for timely dose adjustments, identification of potential complications, and coordination of care across specialties. Nurses and advanced practitioners serve as a bridge between patients and physicians, addressing patient concerns, managing symptoms, and facilitating referrals when needed. By fostering teamwork and prioritizing comprehensive, patient-centered care, the healthcare team can effectively manage Hashimoto thyroiditis as a lifelong condition, ensuring that patients receive the necessary support to maintain thyroid function and overall well-being.
Media
(Click Image to Enlarge)
Hashimoto Thyroiditis. Image demonstrating histological study of the thyroid from a patient with Hashimoto thyroiditis. A commonly described histopathological abnormality in Hashimoto thyroiditis is lymphocytic infiltration and destruction of follicular cells.
Contributed by S Bhimji, MD
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